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In vivo partial reprogramming alters manifestation of age-associated molecular changes in aging mice

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE190986 | GEO | 2022/01/11

REPOSITORIES: GEO

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In vivo partial reprogramming alters manifestation of age-associated molecular changes in aging mice (10 months; long-term treatment)

Project description:Various length of in vivo 4F (four Yamanaka factors) partial reprogramming protocols were performed to evaluate effects of longer-term partial reprogramming in physiologically aging wild-type mice. Here, long-term (10 months) partial reprogramming was induced and transcriptional changes in various tissues were compared to age-matched, untreated mice.

2022-01-11 | GSE190985 | GEO

In vivo partial reprogramming alters manifestation of age-associated molecular changes in aging mice (1 months; sort-term treatment)

Project description:Various length of in vivo 4F (four Yamanaka factors) partial reprogramming protocols were performed to evaluate effects of longer-term partial reprogramming in physiologically aging wild-type mice. Here, short-term (1 months) partial reprogramming was induced and transcriptional changes in various tissues were compared to age-matched, untreated mice.

2022-01-11 | GSE190984 | GEO

In vivo partial reprogramming alters manifestation of age-associated molecular changes in aging mice (7 months; long-term treatment)

Project description:Various length of in vivo 4F (four Yamanaka factors) partial reprogramming protocols were performed to evaluate effects of longer-term partial reprogramming in physiologically aging wild-type mice. Here, long-term (7 months) partial reprogramming was induced and transcriptional changes in various tissues were compared to age-matched, untreated mice.

2022-01-11 | GSE190983 | GEO

In vivo partial reprogramming alters manifestation of age-associated molecular changes in aging mice

Project description:In vivo partial reprogramming alters manifestation of age-associated molecular changes in aging mice

| PRJNA789246 | ENA

In vivo partial reprogramming alters manifestation of age-associated molecular changes in aging mice (1 months; sort-term treatment)

Project description:In vivo partial reprogramming alters manifestation of age-associated molecular changes in aging mice (1 months; sort-term treatment)

| PRJNA789252 | ENA

In vivo partial reprogramming alters manifestation of age-associated molecular changes in aging mice (7 months; long-term treatment)

Project description:In vivo partial reprogramming alters manifestation of age-associated molecular changes in aging mice (7 months; long-term treatment)

| PRJNA789253 | ENA

In vivo partial reprogramming alters manifestation of age-associated molecular changes in aging mice (10 months; long-term treatment)

Project description:In vivo partial reprogramming alters manifestation of age-associated molecular changes in aging mice (10 months; long-term treatment)

| PRJNA789254 | ENA

In Vivo Amelioration of Age-Associated Hallmarks by Partial Reprogramming.

Project description:Aging is the major risk factor for many human diseases. In vitro studies have demonstrated that cellular reprogramming to pluripotency reverses cellular age, but alteration of the aging process through reprogramming has not been directly demonstrated in vivo. Here, we report that partial reprogramming by short-term cyclic expression of Oct4, Sox2, Klf4, and c-Myc (OSKM) ameliorates cellular and physiological hallmarks of aging and prolongs lifespan in a mouse model of premature aging. Similarly, expression of OSKM in vivo improves recovery from metabolic disease and muscle injury in older wild-type mice. The amelioration of age-associated phenotypes by epigenetic remodeling during cellular reprogramming highlights the role of epigenetic dysregulation as a driver of mammalian aging. Establishing in vivo platforms to modulate age-associated epigenetic marks may provide further insights into the biology of aging.

| S-EPMC5679279 | biostudies-literature

Molecular changes associated with spinal cord aging.

Project description:Age-related muscle weakness and loss of muscle mass (sarcopenia) is a universal problem in the elderly. Our previous studies indicate that alpha motor neurons (α-MNs) play a critical role in this process. The goal of the current study is to uncover changes in the aging spinal cord that contribute to loss of innervation and the downstream degenerative processes that occur in skeletal muscle. The number of α-MNs is decreased in the spinal cord of wildtype mice during aging, beginning in middle age and reaching a 41% loss by 27 months of age. There is evidence for age-related loss of myelin and mild inflammation, including astrocyte and microglia activation and an increase in levels of sICAM-1. We identified changes in metabolites consistent with compromised neuronal viability, such as reduced levels of N-acetyl-aspartate. Cleaved caspase-3 is more abundant in spinal cord from old mice, suggesting that apoptosis contributes to neuronal loss. RNA-seq analysis revealed changes in the expression of a number of genes in spinal cord from old mice, in particular genes encoding extracellular matrix components (ECM) and a 172-fold increase in MMP-12 expression. Furthermore, blood-spinal cord barrier (BSCB) permeability is increased in old mice, which may contribute to alterations in spinal cord homeostasis and exacerbate neuronal distress. Together, these data show for the first time that the spinal cord undergoes significant changes during aging, including progressive α-MNs loss that is associated with low-grade inflammation, apoptosis, changes in ECM, myelination, and vascular permeability.

| S-EPMC7205981 | biostudies-literature

Metabolic reprogramming by Acly inhibition using SB-204990 alters glucoregulation and modulates molecular mechanisms associated with aging

Project description:ATP-citrate lyase is a central integrator of cellular metabolism in the interface of protein, carbohydrate, and lipid metabolism. The physiological consequences as well as the molecular mechanisms orchestrating the response to long-term pharmacologically induced Acly inhibition are unknown. We report here that the Acly inhibitor SB-204990 improves metabolic health and physical strength in wild-type mice when fed with a high-fat diet, while in mice fed with healthy diet results in metabolic imbalance and moderated insulin resistance. By applying a multiomic approach using untargeted metabolomics, transcriptomics, and proteomics, we determined that, in vivo, SB-204990 plays a role in the regulation of molecular mechanisms associated with aging, such as energy metabolism, mitochondrial function, mTOR signaling, and folate cycle, while global alterations on histone acetylation are absent. Our findings indicate a mechanism for regulating molecular pathways of aging that prevents the development of metabolic abnormalities associated with unhealthy dieting. This strategy might be explored for devising therapeutic approaches to prevent metabolic diseases.

2023-03-06 | GSE196853 | GEO

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